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Article ; Online: Glutamine Metabolism in Cancer Stem Cells: A Complex Liaison in the Tumor Microenvironment.

Pacifico, Francesco / Leonardi, Antonio / Crescenzi, Elvira

International journal of molecular sciences

2023 Volume 24, Issue 3

Abstract: In this review we focus on the role of glutamine in control of cancer stem cell (CSC) fate. We first provide an overview of glutamine metabolism, and then summarize relevant studies investigating how glutamine metabolism modulates the CSC compartment, ... ...

Abstract	In this review we focus on the role of glutamine in control of cancer stem cell (CSC) fate. We first provide an overview of glutamine metabolism, and then summarize relevant studies investigating how glutamine metabolism modulates the CSC compartment, concentrating on solid tumors. We schematically describe how glutamine in CSC contributes to several metabolic pathways, such as redox metabolic pathways, ATP production, non-essential aminoacids and nucleotides biosynthesis, and ammonia production. Furthermore, we show that glutamine metabolism is a key regulator of epigenetic modifications in CSC. Finally, we briefly discuss how cancer-associated fibroblasts, adipocytes, and senescent cells in the tumor microenvironment may indirectly influence CSC fate by modulating glutamine availability. We aim to highlight the complexity of glutamine's role in CSC, which supports our knowledge about metabolic heterogeneity within the CSC population.
MeSH term(s)	Humans ; Glutamine/metabolism ; Tumor Microenvironment ; Neoplasms/metabolism ; Metabolic Networks and Pathways ; Neoplastic Stem Cells/metabolism
Chemical Substances	Glutamine (0RH81L854J)
Language	English
Publishing date	2023-01-25
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms24032337
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Article: Iron Metabolism in Cancer and Senescence: A Cellular Perspective.

Crescenzi, Elvira / Leonardi, Antonio / Pacifico, Francesco

Biology

2023 Volume 12, Issue 7

Abstract: Iron participates in a number of biological processes and plays a crucial role in cellular homeostasis. Alterations in iron metabolism are considered hallmarks of cancer and drivers of aggressive behaviors, such as uncontrolled proliferation, resistance ... ...

Abstract	Iron participates in a number of biological processes and plays a crucial role in cellular homeostasis. Alterations in iron metabolism are considered hallmarks of cancer and drivers of aggressive behaviors, such as uncontrolled proliferation, resistance to apoptosis, enhanced metastatic ability, increased cell plasticity and stemness. Furthermore, a dysregulated iron metabolism has been associated with the development of an adverse tumor microenvironment. Alterations in iron metabolism have been described in cellular senescence and in aging. For instance, iron has been shown to accumulate in aged tissues and in age-related diseases. Furthermore, in vitro studies demonstrate increases in iron content in both replicative and stress-induced senescent cells. However, the role, the mechanisms of regulation and dysregulation and the effects of iron metabolism on senescence remain significantly less characterized. In this review, we first provide an overview of iron metabolism and iron regulatory proteins. Then, we summarize alterations in iron homeostasis in cancer and senescence from a cellular point of view.
Language	English
Publishing date	2023-07-11
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2661517-4
ISSN	2079-7737
ISSN	2079-7737
DOI	10.3390/biology12070989
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Article ; Online: Iron Metabolism in Cancer and Senescence: A Cellular Perspective

Crescenzi, Elvira / Leonardi, Antonio / Pacifico, Francesco

Biology (Basel). 2023 July 11, v. 12, no. 7

2023

Abstract	Iron participates in a number of biological processes and plays a crucial role in cellular homeostasis. Alterations in iron metabolism are considered hallmarks of cancer and drivers of aggressive behaviors, such as uncontrolled proliferation, resistance to apoptosis, enhanced metastatic ability, increased cell plasticity and stemness. Furthermore, a dysregulated iron metabolism has been associated with the development of an adverse tumor microenvironment. Alterations in iron metabolism have been described in cellular senescence and in aging. For instance, iron has been shown to accumulate in aged tissues and in age-related diseases. Furthermore, in vitro studies demonstrate increases in iron content in both replicative and stress-induced senescent cells. However, the role, the mechanisms of regulation and dysregulation and the effects of iron metabolism on senescence remain significantly less characterized. In this review, we first provide an overview of iron metabolism and iron regulatory proteins. Then, we summarize alterations in iron homeostasis in cancer and senescence from a cellular point of view.
Keywords	apoptosis ; cell senescence ; homeostasis ; iron ; iron absorption ; metastasis ; neoplasms ; plasticity
Language	English
Dates of publication	2023-0711
Publishing place	Multidisciplinary Digital Publishing Institute
Document type	Article ; Online
ZDB-ID	2661517-4
ISSN	2079-7737
ISSN	2079-7737
DOI	10.3390/biology12070989
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: NGAL as a Potential Target in Tumor Microenvironment.

Crescenzi, Elvira / Leonardi, Antonio / Pacifico, Francesco

International journal of molecular sciences

2021 Volume 22, Issue 22

Abstract: The signaling network between cancer and stromal cells plays a crucial role in tumor microenvironment. The fate of tumor progression mainly depends on the huge amount of information that these cell populations exchange from the onset of neoplastic ... ...

Abstract	The signaling network between cancer and stromal cells plays a crucial role in tumor microenvironment. The fate of tumor progression mainly depends on the huge amount of information that these cell populations exchange from the onset of neoplastic transformation. Interfering with such signaling has been producing exciting results in cancer therapy: just think of anti-PD-1/anti-PD-L1/anti-CTLA-4 antibodies that, acting as immune checkpoint inhibitors, interrupt the inhibitory signaling exerted by cancer cells on immune cells or the CAR-T technology that fosters the reactivation of anti-tumoral immunity in a restricted group of leukemias and lymphomas. Nevertheless, many types of cancers, in particular solid tumors, are still refractory to these treatments, so the identification of novel molecular targets in tumor secretome would benefit from implementation of current anti-cancer therapeutical strategies. Neutrophil Gelatinase-Associated Lipocalin (NGAL) is a secreted protein abundantly expressed in the secretome of various human tumors. It represents a promising target for the multiple roles that are played inside cancer and stromal cells, and also overall in their cross-talk. The review focuses on the different roles of NGAL in tumor microenvironment and in cancer senescence-associated secretory phenotype (SASP), highlighting the most crucial functions that could be eventually targetable in cancer therapy.
MeSH term(s)	Animals ; Antibodies, Monoclonal/therapeutic use ; CRISPR-Cas Systems ; Gene Editing/methods ; Humans ; Lipocalin-2/antagonists & inhibitors ; Lipocalin-2/genetics ; Lipocalin-2/immunology ; Lipocalin-2/metabolism ; Neoplasms/metabolism ; Neoplasms/therapy ; RNA, Small Interfering/genetics ; RNAi Therapeutics/methods ; Secretome/metabolism ; Senescence-Associated Secretory Phenotype ; Signal Transduction/drug effects ; Signal Transduction/genetics ; Stromal Cells/metabolism ; Tumor Microenvironment
Chemical Substances	Antibodies, Monoclonal ; LCN2 protein, human ; Lipocalin-2 ; RNA, Small Interfering
Language	English
Publishing date	2021-11-15
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms222212333
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Article ; Online: Analysis of the Contribution of NF-κB in the Regulation of Chemotherapy-Induced Cell Senescence by Establishing a Tetracycline-Regulated Cell System.

Pacifico, Francesco / Crescenzi, Elvira / Leonardi, Antonio

Methods in molecular biology (Clifton, N.J.)

2021 Volume 2366, Page(s) 193–212

Abstract: Therapy-induced senescence (TIS or therapy-induced premature senescence) is a key cellular program triggered in the course of cancer radiotherapy and chemotherapy with genotoxic drugs, both in cancer cells and in normal cells, whose activation critically ...

Abstract	Therapy-induced senescence (TIS or therapy-induced premature senescence) is a key cellular program triggered in the course of cancer radiotherapy and chemotherapy with genotoxic drugs, both in cancer cells and in normal cells, whose activation critically affects the outcome of cancer therapy. Drug-induced senescent cells undergo a permanent cell cycle arrest, acquire distinctive morphological and biochemical alterations, and an enhanced secretory ability, referred to as senescence-associated secretory phenotype (SASP). The transcription factor NF-κB acts as a master regulator of the SASP, driving the expression of senescence-associated secretome components.Here we describe protocols for the establishment of a tetracycline-regulated cell system for the investigation of the role of NF-κB in TIS. We also describe protocols routinely used in our laboratory, to investigate TIS in this Tet-On inducible expression system. Finally, we describe techniques for the validation of TIS induction.
MeSH term(s)	Antineoplastic Agents/pharmacology ; Cellular Senescence/drug effects ; NF-kappa B/genetics ; NF-kappa B/metabolism ; Protein Synthesis Inhibitors/pharmacology ; Secretome ; Senescence-Associated Secretory Phenotype ; Tetracycline/pharmacology
Chemical Substances	Antineoplastic Agents ; NF-kappa B ; Protein Synthesis Inhibitors ; Tetracycline (F8VB5M810T)
Language	English
Publishing date	2021-07-08
Publishing country	United States
Document type	Journal Article
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-0716-1669-7_12
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Article ; Online: NGAL Mediates Anaplastic Thyroid Carcinoma Cells Survival Through FAS/CD95 Inhibition.

Crescenzi, Elvira / Mellone, Stefano / Gragnano, Gianluca / Iaccarino, Antonino / Leonardi, Antonio / Pacifico, Francesco

Endocrinology

2023 Volume 165, Issue 2

Abstract: Neutrophil gelatinase-associated lipocalin (NGAL), a siderophore-mediated iron binding protein, is highly expressed in human anaplastic thyroid carcinomas (ATCs) where it plays pleiotropic protumorigenic roles including that of a prosurvival protein. ... ...

Abstract	Neutrophil gelatinase-associated lipocalin (NGAL), a siderophore-mediated iron binding protein, is highly expressed in human anaplastic thyroid carcinomas (ATCs) where it plays pleiotropic protumorigenic roles including that of a prosurvival protein. Here we show that NGAL inhibits FAS/CD95 death receptor to control ATC cell survival. FAS/CD95 expression in human specimens from patients with ATC and in ATC-derived cell lines negatively correlate with NGAL expression. Silencing of NGAL in ATC cells leads to FAS/CD95 upregulation, whereas NGAL overexpression determines the opposite effect. As a result, an agonist anti-FAS/CD95 antibody induces cell death in NGAL-silenced cells while it is ineffective on NGAL-overexpressing cells. Interestingly, the inhibitory activity of NGAL on FAS/CD95 is due to its iron carrier property given that perturbing iron homeostasis of NGAL-proficient and -deficient ATC cells directly influences FAS/CD95 expression. Accordingly, conditioned media containing a mutant form of NGAL unable to bind siderophores cannot rescue cells from FAS/CD95-dependent death, whereas NGAL wild type-containing conditioned media abolish the effects of the agonist antibody. We also find that downregulation of FAS/CD95 expression is mediated by iron-dependent NGAL suppression of p53 transcriptional activity. Our results indicate that NGAL contributes to ATC cell survival by iron-mediated inhibition of p53-dependent FAS/CD95 expression and suggest that restoring FAS/CD95 by NGAL suppression could be a helpful strategy to kill ATC cells.
MeSH term(s)	Humans ; Lipocalin-2/genetics ; Thyroid Carcinoma, Anaplastic ; Proto-Oncogene Proteins/metabolism ; Tumor Suppressor Protein p53 ; Cell Survival ; Culture Media, Conditioned ; Iron ; Thyroid Neoplasms/genetics ; Thyroid Neoplasms/pathology ; Apoptosis ; fas Receptor/genetics ; fas Receptor/metabolism
Chemical Substances	Lipocalin-2 ; Proto-Oncogene Proteins ; Tumor Suppressor Protein p53 ; Culture Media, Conditioned ; Iron (E1UOL152H7) ; fas Receptor
Language	English
Publishing date	2023-12-13
Publishing country	United States
Document type	Journal Article
ZDB-ID	427856-2
ISSN	1945-7170 ; 0013-7227
ISSN (online)	1945-7170
ISSN	0013-7227
DOI	10.1210/endocr/bqad190
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Article ; Online: Trabectedin suppresses escape from therapy-induced senescence in tumor cells by interfering with glutamine metabolism.

Pacifico, Francesco / Mellone, Stefano / D'Incalci, Maurizio / Stornaiuolo, Mariano / Leonardi, Antonio / Crescenzi, Elvira

Biochemical pharmacology

2022 Volume 202, Page(s) 115159

Abstract: Conventional and targeted cancer therapies may induce a cellular senescence program termed therapy-induced senescence. However, unlike normal cells, cancer cells are able to evade the senescence cell cycle arrest and to resume proliferation, driving ... ...

Abstract	Conventional and targeted cancer therapies may induce a cellular senescence program termed therapy-induced senescence. However, unlike normal cells, cancer cells are able to evade the senescence cell cycle arrest and to resume proliferation, driving tumor recurrence after treatments. Cells that escape from therapy-induced senescence are characterized by a plastic, cancer stem cell-like phenotype, and recent studies are beginning to define their unique metabolic features, such as glutamine dependence. Here, we show that the antineoplastic drug trabectedin suppresses escape from therapy-induced senescence in all cell lines studied, and reduces breast cancer stem-like cells, at concentrations that do not affect the viability of senescent tumor cells. We demonstrate that trabectedin downregulates both the glutamine transporter SLC1A5 and glutamine synthetase, thereby interfering with glutamine metabolism. On the whole, our results indicate that trabectedin targets a glutamine-dependent cancer stem-like cell population involved in evasion from therapy-induced senescence and suggest a therapeutic potential for trabectedin combined with pro-senescence chemotherapy in tumor treatment.
MeSH term(s)	Amino Acid Transport System ASC/genetics ; Amino Acid Transport System ASC/metabolism ; Cell Cycle Checkpoints ; Cell Line, Tumor ; Cellular Senescence/physiology ; Glutamine/metabolism ; Humans ; Minor Histocompatibility Antigens/genetics ; Neoplasms/metabolism ; Neoplastic Stem Cells/pathology ; Trabectedin
Chemical Substances	Amino Acid Transport System ASC ; Minor Histocompatibility Antigens ; SLC1A5 protein, human ; Glutamine (0RH81L854J) ; Trabectedin (ID0YZQ2TCP)
Language	English
Publishing date	2022-06-30
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	208787-x
ISSN	1873-2968 ; 0006-2952
ISSN (online)	1873-2968
ISSN	0006-2952
DOI	10.1016/j.bcp.2022.115159
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Article ; Online: Glutamine promotes escape from therapy-induced senescence in tumor cells.

Pacifico, Francesco / Badolati, Nadia / Mellone, Stefano / Stornaiuolo, Mariano / Leonardi, Antonio / Crescenzi, Elvira

Aging

2021 Volume 13, Issue 17, Page(s) 20962–20991

Abstract: Therapy-induced senescence (TIS) is a major cellular response to anticancer therapies. While induction of a persistent growth arrest would be a desirable outcome in cancer therapy, it has been shown that, unlike normal cells, cancer cells are able to ... ...

Abstract	Therapy-induced senescence (TIS) is a major cellular response to anticancer therapies. While induction of a persistent growth arrest would be a desirable outcome in cancer therapy, it has been shown that, unlike normal cells, cancer cells are able to evade the senescence cell cycle arrest and to resume proliferation, likely contributing to tumor relapse. Notably, cells that escape from TIS acquire a plastic, stem cell-like phenotype. The metabolic dependencies of cells that evade senescence have not been thoroughly studied. In this study, we show that glutamine depletion inhibits escape from TIS in all cell lines studied, and reduces the stem cell subpopulation. In line with a metabolic reliance on glutamine, escaped clones overexpress the glutamine transporter SLC1A5. We also demonstrate a central role of glutamine synthetase that mediates resistance to glutamine deprivation, conferring independence from exogenous glutamine. Finally, rescue experiments demonstrate that glutamine provides nitrogen for nucleotides biosynthesis in cells that escape from TIS, but also suggest a critical involvement of glutamine in other metabolic and non-metabolic pathways. On the whole, these results reveal a metabolic vulnerability of cancer stem cells that recover proliferation after exposure to anticancer therapies, which could be exploited to prevent tumor recurrence.
MeSH term(s)	A549 Cells ; Amino Acid Transport System ASC/metabolism ; Cell Cycle Checkpoints ; Cell Proliferation ; Cellular Senescence ; Enzyme Activation ; Glutamate-Ammonia Ligase/metabolism ; Glutamine/metabolism ; Humans ; MCF-7 Cells ; Minor Histocompatibility Antigens/metabolism ; Neoplasm Recurrence, Local/etiology ; Neoplasm Recurrence, Local/metabolism ; Neoplasm Recurrence, Local/prevention & control ; Neoplasms/drug therapy ; Neoplasms/metabolism ; Neoplastic Stem Cells ; Nitrogen/metabolism ; Nucleotides/biosynthesis ; Senescence-Associated Secretory Phenotype ; Tumor Escape
Chemical Substances	Amino Acid Transport System ASC ; Minor Histocompatibility Antigens ; Nucleotides ; SLC1A5 protein, human ; Glutamine (0RH81L854J) ; Glutamate-Ammonia Ligase (EC 6.3.1.2) ; Nitrogen (N762921K75)
Language	English
Publishing date	2021-09-07
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1945-4589
ISSN (online)	1945-4589
DOI	10.18632/aging.203495
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Article ; Online: Thyroid hormone and androgen signals mutually interplay and enhance inflammation and tumorigenic activation of tumor microenvironment in prostate cancer.

Miro, Caterina / Di Giovanni, Angelo / Murolo, Melania / Cicatiello, Annunziata Gaetana / Nappi, Annarita / Sagliocchi, Serena / Di Cicco, Emery / Morra, Francesco / Celetti, Angela / Pacifico, Francesco / Imbimbo, Ciro / Crocetto, Felice / Dentice, Monica

Cancer letters

2022 Volume 532, Page(s) 215581

Abstract: Prostate Cancer (PCa) is the most commonly diagnosed non-cutaneous cancer in males and the fifth leading cause of death worldwide. The majority of PCas are androgen-sensitive, with a significant up-regulation of Androgen Receptor (AR) that causes a ... ...

Abstract	Prostate Cancer (PCa) is the most commonly diagnosed non-cutaneous cancer in males and the fifth leading cause of death worldwide. The majority of PCas are androgen-sensitive, with a significant up-regulation of Androgen Receptor (AR) that causes a stimulatory effect on growth and progression of cancer cells. For this reason, the first-line therapy for PCa is androgen ablation, even if it ultimately fails due to the onset of hormone-refractory state, in which the malignant cells do not sense the androgen signal anymore. Besides androgens, a growing number of evidence suggests that Thyroid Hormones (THs) mediate tumor-promoting effects in a variety of human cancers, as Epithelial-to-Mesenchymal Transition (EMT), invasion and metastasis and also stimulation of angiogenesis and tumor metabolism. Moreover, epidemiological studies demonstrated an increased risk for PCa in patients with lower levels of Thyreotropin (TSH). Here, we investigated if intracellular TH metabolism affects Benign Prostatic Hyperplasia (BPH) and PCa formation and progression. We found that the intracellular TH metabolism is a crucial determinant of PCa behavior. We observed that a dynamic stage-specific expression of the THs modulating enzymes, the deiodinases, is required for the progression of BPH to PCa malignancy. By acting simultaneously on epithelial cancer cells and fibroblasts, THs exert a proliferative and pro-inflammatory effect cooperating with androgens. These findings suggest that androgens and THs may interplay and mediate a coordinate effect on human PCa formation and progression. In light of our results, future perspective could be to explore the potential benefits of THs intracellular modulators aimed to counteract PCa progression.
MeSH term(s)	Androgens/metabolism ; Carcinogenesis ; Cell Line, Tumor ; Humans ; Inflammation ; Male ; Prostatic Hyperplasia/metabolism ; Prostatic Hyperplasia/pathology ; Prostatic Neoplasms/pathology ; Receptors, Androgen/metabolism ; Thyroid Hormones ; Tumor Microenvironment
Chemical Substances	Androgens ; Receptors, Androgen ; Thyroid Hormones
Language	English
Publishing date	2022-02-05
Publishing country	Ireland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	195674-7
ISSN	1872-7980 ; 0304-3835
ISSN (online)	1872-7980
ISSN	0304-3835
DOI	10.1016/j.canlet.2022.215581
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Article ; Online: NGAL promotes recruitment of tumor infiltrating leukocytes.

Pacifico, Francesco / Pisa, Luna / Mellone, Stefano / Cillo, Michele / Lepore, Alessio / Leonardi, Antonio

Oncotarget

2018 Volume 9, Issue 56, Page(s) 30761–30772

Abstract: We have previously shown that Neutrophil Gelatinase-Associated Lipocalin (NGAL) is strongly expressed in thyroid carcinomas, especially of anaplastic type, where it protects neoplastic cells from serum deprivation-induced apoptosis and enhances tumor ... ...

Abstract	We have previously shown that Neutrophil Gelatinase-Associated Lipocalin (NGAL) is strongly expressed in thyroid carcinomas, especially of anaplastic type, where it protects neoplastic cells from serum deprivation-induced apoptosis and enhances tumor invasivity by regulating MMP-9 activity. Here we demonstrate that NGAL-containing conditioned medium from human anaplastic thyroid carcinoma (ATC) cells is able to induce monocyte migration
Language	English
Publishing date	2018-07-20
Publishing country	United States
Document type	Journal Article
ZDB-ID	2560162-3
ISSN	1949-2553 ; 1949-2553
ISSN (online)	1949-2553
ISSN	1949-2553
DOI	10.18632/oncotarget.25625
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